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STEP Pharm I > DMARDs > Flashcards

DMARDs Flashcards

1
Q

The treatment of RA is progressive. What do most clinicians start with?

A

a DMARD like METHOTREXATE with the addition of an NSAID and a corticosteroid

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2
Q

How is RA treated initiated in milder cases?

A

Hydroxychloroquine is preferred because of lower toxicity

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3
Q

What is considered in RA treatment after initial treatment failure?

A

a first-line biological agent such as Etanercept, Infliximab, Adalimumab, Golimumab, or Certolizumab

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4
Q

T or F. Experience shows that early, aggressive treatment with MTX and/or a biological agent results in longer disease-free remission, less joint destruction, and a better quality of life

A

T.

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5
Q

What are the results of Methotrexate use?

A

inhibition of lymphocyteproliferation and suppression of several pro-inflammatory mediators (Il-1, IFN-y, and TNF) via tonic adenosine activation.

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6
Q

What process does Methotrexate undergo that helps retain it in the cell?

A

polyglutamation

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7
Q

High-dose methotrexate therapy is associated with what?

A

bone marrow suppression, although this may not be problematic at doses used in the treatment of arthritis.

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8
Q

How is Methotrexate metabolized?

A

hepatic (contraindicated with alcoholism, or other hepatic disease)

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9
Q

How is Methotrexate eliminated?

A

renal (hydrate and alkalination to avoid damage)

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10
Q

AEs of Methotrexate?

A

-opportunistic infection, tumor -malignant lymphoma-derm rxns -severe GI toxicity -irreversible pulmonary fibrosis

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11
Q

What can increase the risk of Gi toxicity with methotrexate use?

A

concurrent NSAID use

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12
Q

Is Methotrexate safe in pregnancy or breast-feeding?

A

No, category X

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13
Q

T or F. Vaccinations should be avoided while on methotrexate

A

T. Ab response may be suboptimal

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14
Q

How is Sulfasalazine metabolized?

A

to sulfapyridine and melamine by colon bacteria which are then acetylated and hydroxylated in the liver (look out for slow acetylators)

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15
Q

How does Sulfasalazine help in RA?

A

anti-inflammatory properties from melamine, an inhibitor of PG and leukotriene production

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16
Q

How is Sulfasalazine eliminated?

A

renal

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17
Q

Contraindications of Sulfasalazine?

A

PMH of hypersensitivity to salicylate or sulfonamide drugs

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18
Q

AEs of Sulfasalazine?

A

fatal blood dyscrasia

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19
Q

How does Leflunomide work?

A

inhibits dihydroorotate dehydrogenase, a mitochondrial enzyme that catalyzed a key step in de novo pyrimidine synthesis causing cell cycle arrest in T/B lymphocytes

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20
Q

Is Leflunomide safe in pregnancy?

A

no, category X

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21
Q

T or F. Leflunomide metabolites produce a uricosuric effect

A

T. that is, it increases the renal elimination of uric acid

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22
Q

How is Hydroxychloroquine used for RA treatment (note it is also used for malaria and SLE treatment)?

A

increases intracellular vacuole pH thus inhabiting the acidic cytoplasmic compartments required for antigenic protein digestion and peptide assembly with the alpha and beta chains of MCH class II proteins

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23
Q

AEs of Hydroxychloroquine?

A

-blood dyscrasia-CNS toxicity (seizures, ototoxicity, polyneuritis)-rarely causes coral opacities, retinopathy, or keratopathy

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24
Q

Contraindications to Hydroxychloroquine use?

A

-hepatic disease (concentrates in liver normally)-ocular disease

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25
Q

Monitoring parameters for Methotrexate?

A

CBC with differential, LFT, serum creatine/BUN, pregnancy testand serum uric acid

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26
Q

Monitoring parameters for Sulfasalazine?

A

CBC with differential, LFT, serum creatine/BUN and urinalysis

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27
Q

Monitoring parameters for Leflunamide?

A

CBC with differential, LFT, pregnancy test and serum electrolytes

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28
Q

Monitoring parameters for Hydroxychloroquine?

A

CBC and opthalmalogic exam

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29
Q

How do corticosteroids work?

A

Nf-kB, activator protein (AP)-1 and NF-AT all inhibited leading to reduced production of TNF-a, IL-1, and thus IL-6 ANDother mechanisms

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30
Q

Mechanism of some AEs of corticosteroids?

A

upregulation of receptor-activator of nuclear factor kB (RANKL) and macrophage colony-stimulating factor (MCF) and down regulation of osteoprotegerin

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31
Q

What does upregulation of RANKL and macrophage colony-stimulating factor (MCF) cause?

A

increased osteoclast production (and lifespan) leading to increased bone resorption early in GC treatment (and transiently)

32
Q

How do GCs affect osteoblasts?

A

upregulate PPARy2 expression and decrease Wnt signaling leading to decreased osteoblastogenesis ANDupregulate caspase 3 expression

33
Q

What is the effect of decreased osteoblast populations?

A

these effects are responsible for the LONG TERM state of decreased been formation that characteristic of GC-induced osteoporosis

34
Q

T or F. In addition to suppressing symptoms/signs of early RA, GCs appear to possess disease-modifying effects, at least in early stage disease

A

T.

35
Q

What are some things that can be done to prevent GC-induce osteoporosis?

A

-advice sufficient dietary intake of calcium, protein, and vitamin D-weight-bearing exercise -avoid alcohol and tobacco abuse

36
Q

What treatment options are available to those chronically taking GCs to reduce risk of osteoporosis?

A

anti-osteoporotic therapy in those with fracture risk (measure height annually and assess BMD regularly)

37
Q

AEs of high-dose GCs?

A

-Cushingoid (w/ HTN) syndrome-diabetes mellitus-cataracts-growth retardation

38
Q

Clinical studies clearly show that patients with rheumatoid arthritis are at increasedrisk of _________ compared to the general population.

A

cardiovascular events. This might be due to the inflammatory condition that the patient is experiencing, but it could also beattributed to adverse effects of drugs used in the treatment of the condition.

39
Q

What is one way to avoid the general systemic effects of corticosteroids?

A

Administer suchdrugs by injection, for example as intra-articular injection in the knee

40
Q

T or F. Adverse effects of corticosteroids are both cumulative and daily dose dependent and can be influenced by the concurrent administration and other drugs such as DMARDs.

A

T. However, low-dose corticosteroids do not necessarily produce the myriad of adverse effects and may be used quite safely with routine clinical care.

41
Q

Still, what should be monitored with low-dose GC?

A

osteoporosis, blood sugar levels, glaucoma and the presence of oedema.

42
Q

What is Auranofin?

A

old RA drug composed of golf that suppressed inflammation but is accompanied by skin rash and GI dysfunction and is not sued anymore here may have use in other diseases

43
Q

What is Abatacept (Orencia)?

A

Fusion protein of human CTLA4/IgG1 Fc Fragment that binds CD80 and CD86 and prevents T-cell co-stimulatory signal engaging with CD28

44
Q

What is Adalimumab (Humira)?

A

TNF-a monoclonal Ab, blocking its interaction with the p55 and p75 cell surface receptors

45
Q

What is Anakinra?

A

recombinant human IL-1 receptor antagonist

46
Q

What is Certolizumab peg?

A

Fab fragment of humanized TNF-a Ab the neutralized membrane-associated and soluble human TNF-a

47
Q

What is Etancercept?

A

Extracellular ligand-binding portion of human p75 TNF receptor linked to part of human IgG Fc

48
Q

What is the role of endogenous p75?

A

TNF antagonist

49
Q

What is the effect of Etancercept (Enbrel)?

A

it binds to and inactivates TNF but does not affect TNF production or serum levels

50
Q

What is Golimumab (Simponi)

A

Human-Derived TNF-a Ab (V and C regions) that binds to and neutralizes both soluble and transmembrane TNF-a

51
Q

What is Infliximab (Remicade)?

A

Chimeric (mouse-human) IgGk monoclonal Ab against TNF-a that binds and neutralizes both soluble and transmembrane TNF-a

52
Q

What is Tocilizumab (Actemra)?

A

Humanized IL-6 receptor-inhibiting monoclonal Ab that binds to soluble (serum and synovial fluid) and membrane-bound IL-6 and inhibits signaling

53
Q

What is Rituximab (Rituxan)?

A

Chimeric monoclonal against CD20 on B cells

54
Q

How does Rituximab work?

A

Fab domain binds CD20 and Fc domain recruits immune effectors to meidate B-cell lysis (ADCC, Ab-dependent, etc.)

55
Q

Rules of thumb with biologics

A

-don’t initiate treatment during infection-may increase infection or malignancy risk

56
Q

Which biologics can cause CHF or hypotension /angina/dysrhythmia?

A

-Infliximab (contraindicated)-Adalimumab-Golimumab-Rituximab

57
Q

Which biologics can cause a lupus-like presentation?

A

-Adalimumab-Certolizumab-Etanercept-Infliximab

58
Q

Stevens-Johnson syndrome (toxic epidermal necrolysis) has been infrequently reported with _____

A

Rituximab

59
Q

What biologic may fuck with blood glucose tests?

A

Abatacept IV (contains maltose)

60
Q

T or F. Women taking Rituximab must use reliable contraception while taking the drug and avoid pregnancy for 4-6 months after therapy

A

T. IgG crosses placenta and could deplete B-cells

61
Q

Which biologics cannot be given SC?

A

-Infliximab-Rituximab-Tocilizumab all others have the risk for injection site reactions with repeated injection given in the same spot

62
Q

CBCs should be routinely given with which biologics? Why?

A

-Anakinra, Certolizumab, Rituximab, Tocilizumab due to risk of blood dyscrasia

63
Q

CBCs should be routinely monitored with which biologics? Why?

A

Golimumab, Infliximab, and Tocilimumab

64
Q

Give a serum lipid profile with which biologic?

A

Tocilizumab

65
Q

What is Tofacitinib (Xeljanz)?

A

Po JAK3/JAK1 inhibitor for mild-severe RA

66
Q

What interleukins are blocked by Tofacitinib?

A

IL-2, 4, 7, 9, 15, and 21

67
Q

AEs of Xeljanz?

A

increased HDL and LDL cholesterol, headache, UTIs, URTIs, nasopharyngitis

68
Q

BBWs of Xeljanz?

A

-serious infections, including Tb and opportunistic -Lymphoma

69
Q

What is Apremilast (Otezla)?

A

an orally (CYP) active phosphodiesterase inhibitor (PDE4), giving rise to a reduction in pro inflammatorymediators

70
Q

Uses for Apremilast?

A

psoriatic arthritis (improves joint tenderness and swelling) and plaque psoriasis (redness/scaliness).

71
Q

AES of Otezla?

A

Nausea, headache, weight loss (monitor!), depression/suicidal ideation rarely

72
Q

What drugs should be avoided in G6PD deficient patients?

A

Sulfasalazine and Hydroxycloroquine (look for hemolytic anemia)

73
Q

What are the 4 mechanisms for the inhibition of TNF-a bearing cells by anti-TNF agents?

A
  1. inhibition of TNF signalingDestruction of TNFa bearing cells by:2. CDC3. ADCC and4. outside-to-inside signal (reverse signaling)
74
Q

What is TAILS?

A

TNF-a antagonist-induced lupus like syndrome thought to be due to release of antigenic particles during apoptosis, stimulating autoantibodies or by suppressing Th1 usually abates 1-6 months when drug stopped

75
Q

T or F. TNF levels are elevated in CHF patients

A

T. BUT TNF-a antagonists only make it worse!!! AVOID

STEP Pharm I (36 decks)

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